New research is revealing some alarming concerns over the safety of Statin agents and questioning their effectiveness in a high percentage of patients taking these drugs.
How do Statins Work? The process of producing cholesterol begins with a two carbon molecule, acetyl-CoA, known as the "building block of life." Acetyl-CoA molecules combine to form hydroxymethyl glutaric acid (HMG). The enyme HMG-CoA reductase is required for mevalonate to be produced from HMG-CoA reductase. Statin drugs inhibit this enzyme and that is why they are known as HMG-CoA reductase inhibitors. This is the reason for the reported numerous side effects.
Statin drugs don't just inhibit the production of cholesterol. Statins inhibit the production of an entire group of intermediary enzymes and molecules that have essential biochemical functions. The mevalonate chain produces 3 end products and one of those is Cholesterol. Ubiquinone and dolichol are the others.
Ubiquinone also known as Co-Enzyme Q10 is an essential cellular nutrient formed in the mitochondria and is necessary for ATP production, functioning as an electron transporter to cytochrome oxidase, the primary respiratory enzyme. High levels of Co-Q10 are required by the heart to function. Ubiquinone, a form of Co-Q10 is in all cell membranes where it plays a vital role in maintaining proper cell membrane structure for nerves and muscles to function. Reduction in serum Ubiquinone levels have been described after statin therapy
Proteins are synthesized within the membranes of the endoplasmic reticulum. This complex creation of peptides is directed by dolichol phosphate. The Dolichols are also critical in the assembly of glycoproteins, which allow complex protein structures to fold and interact with receptors and membranes. Dolichol-mediated processes create complex neuropeptides, and mechanisms critical in cellular communication, identification, and immune function. The reality of Dolichol inhibition by statin agents is evident and the resultant turmoil in cellular function is not unexpected. It is also not unexpected that altered cognition and abnormal behavior can result from statin induced neuropeptide formation.
Drastic Cholesterol Reduction. It seems that a lot of these problems begin when cholesterol levels become elevated and aggressive reduction occurs with the use of statin agents. Therefore elevated cholesterol levels have been described as the initiating phase in the development of atherosclerosis. Of course, statins inhibit the production of cholesterol--they do this very well. Cholesterol is the body's repair substance: scar tissue contains high levels of cholesterol, including scar tissue in the arteries. Cholesterol is the precursor to vitamin D, necessary for numerous biochemical processes including mineral metabolism. The use of statin agents will reduce the synthesis of Vitamin D. Studies have identified the increased incidence of musculoskeletal pain in patients who are vitamin D deficient, and that replacement results in dramatic improvement.
A number of patients describe gastrointestinal symptoms and diarrhea associated with statin therapy. Unfortunately after an extensive gastrointestinal workup, the statin therapy is not discontinued. Statin agents reduce bile salts production, which is required for the digestion of fat. Those who suffer from low cholesterol often have trouble digesting fats. Cholesterol also functions as a powerful antioxidant, thus protecting us against cancer and aging.
It is no surprise that the aggressive control of cholesterol, typical of statin therapy, in an attempt to reduce cardiovascular disease, in itself produces it's own disease process. Even though statins have not been proven to decrease the risk of heart attacks and strokes for those not suffering from heart disease.
How do Statins Work? The process of producing cholesterol begins with a two carbon molecule, acetyl-CoA, known as the "building block of life." Acetyl-CoA molecules combine to form hydroxymethyl glutaric acid (HMG). The enyme HMG-CoA reductase is required for mevalonate to be produced from HMG-CoA reductase. Statin drugs inhibit this enzyme and that is why they are known as HMG-CoA reductase inhibitors. This is the reason for the reported numerous side effects.
Statin drugs don't just inhibit the production of cholesterol. Statins inhibit the production of an entire group of intermediary enzymes and molecules that have essential biochemical functions. The mevalonate chain produces 3 end products and one of those is Cholesterol. Ubiquinone and dolichol are the others.
Ubiquinone also known as Co-Enzyme Q10 is an essential cellular nutrient formed in the mitochondria and is necessary for ATP production, functioning as an electron transporter to cytochrome oxidase, the primary respiratory enzyme. High levels of Co-Q10 are required by the heart to function. Ubiquinone, a form of Co-Q10 is in all cell membranes where it plays a vital role in maintaining proper cell membrane structure for nerves and muscles to function. Reduction in serum Ubiquinone levels have been described after statin therapy
Proteins are synthesized within the membranes of the endoplasmic reticulum. This complex creation of peptides is directed by dolichol phosphate. The Dolichols are also critical in the assembly of glycoproteins, which allow complex protein structures to fold and interact with receptors and membranes. Dolichol-mediated processes create complex neuropeptides, and mechanisms critical in cellular communication, identification, and immune function. The reality of Dolichol inhibition by statin agents is evident and the resultant turmoil in cellular function is not unexpected. It is also not unexpected that altered cognition and abnormal behavior can result from statin induced neuropeptide formation.
Drastic Cholesterol Reduction. It seems that a lot of these problems begin when cholesterol levels become elevated and aggressive reduction occurs with the use of statin agents. Therefore elevated cholesterol levels have been described as the initiating phase in the development of atherosclerosis. Of course, statins inhibit the production of cholesterol--they do this very well. Cholesterol is the body's repair substance: scar tissue contains high levels of cholesterol, including scar tissue in the arteries. Cholesterol is the precursor to vitamin D, necessary for numerous biochemical processes including mineral metabolism. The use of statin agents will reduce the synthesis of Vitamin D. Studies have identified the increased incidence of musculoskeletal pain in patients who are vitamin D deficient, and that replacement results in dramatic improvement.
A number of patients describe gastrointestinal symptoms and diarrhea associated with statin therapy. Unfortunately after an extensive gastrointestinal workup, the statin therapy is not discontinued. Statin agents reduce bile salts production, which is required for the digestion of fat. Those who suffer from low cholesterol often have trouble digesting fats. Cholesterol also functions as a powerful antioxidant, thus protecting us against cancer and aging.
It is no surprise that the aggressive control of cholesterol, typical of statin therapy, in an attempt to reduce cardiovascular disease, in itself produces it's own disease process. Even though statins have not been proven to decrease the risk of heart attacks and strokes for those not suffering from heart disease.
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